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Oncogene-dependent apoptosis is mediated by caspase-9.
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| Author |
Fearnhead, H O, et al. |
| Citation Information |
Proc. Natl. Acad. Sci. U.S.A., 95: 13664-9 (1998), : (1998) |
| Related Products |
05-654, 05-573, 05-572 |
| Pub Med ID |
9811857 |
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Abstract
Understanding how oncogenic transformation sensitizes cells to apoptosis may provide a strategy to kill tumor cells selectively. We previously developed a cell-free system that recapitulates oncogene dependent apoptosis as reflected by activation of caspases, the core of the apoptotic machinery. Here, we show that this activation requires a previously identified apoptosis-promoting complex consisting of caspase-9, APAF-1, and cytochrome c. As predicted by the in vitro system, preventing caspase-9 activation blocked drug-induced apoptosis in cells sensitized by E1A, an adenoviral oncogene. Oncogenes, such as E1A, appear to facilitate caspase-9 activation by several mechanisms, including the control of cytochrome c release from the mitochondria.
